Bipolar disorder moderates associations between linoleic acid and markers of inflammation

Ya Wen Chang, Shervin Assari, Alan R. Prossin, Laura Stertz, Melvin G. McInnis, Simon J. Evans

Research output: Research - peer-reviewArticle

Abstract

Dietary polyunsaturated fatty acids (PUFA) and inflammatory proteins associate with immune activation and have been implicated in the pathophysiology of mood disorders. We have previously reported that individuals with bipolar disorder (BPD) have decreased PUFA intake, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and arachidonic acid (AA); and decreased PUFA concentration of plasma EPA and linoleic acid (LA). We have also reported an association between plasma LA and its metabolites and burden of disease measures in BPD. In the current cross-sectional study we collected blood samples and diet records from both bipolar (n = 91) and control subjects (n = 75) to quantify plasma cytokine concentrations and dietary LA intake, respectively. Using multiple linear regression techniques, we tested for case control differences in plasma cytokine levels and associations between cytokines and dietary LA intake, adjusting for sex, age, BMI, and total energy intake. We found significantly higher plasma levels of interleukin 18 (IL-18) (p = 0.036), IL-18 binding protein (IL-18BP) (p = 0.001), soluble tumor necrosis factor receptor (sTNFR) 1 (p = 0.006), and sTNFR2 (p = 0.007) in BPD compared with controls. Moreover, BPD significantly moderated the associations of dietary LA intake with plasma levels of IL-18, sTNFR1 and sTNFR2, which were inverse associations in bipolar individuals and positive associations in controls (p for dietary LA x BPD diagnosis interaction < 0.05 for all three). These findings suggest potential dysregulation of LA metabolism in BPD, which may extend to a modified influence of dietary LA on specific inflammatory pathways in individuals with BPD compared to healthy controls.

LanguageEnglish (US)
Pages29-36
Number of pages8
JournalJournal of Psychiatric Research
Volume85
DOIs
StatePublished - Feb 1 2017
Externally publishedYes

Fingerprint

Bipolar Disorder
Inflammation
Linoleic Acid
Plasma
Intake
Fatty Acids
Unsaturated Fatty Acids
Cytokines
Protein
Interleukin-18
Eicosapentaenoic Acid
Diet
Pathway
Burden
Interaction
Blood
Metabolism
Mood Disorders
Energy
Activation

Keywords

  • Bipolar disorder
  • Interleukin
  • Linoleic acid
  • Tumor necrosis factor receptor

ASJC Scopus subject areas

  • Arts and Humanities (miscellaneous)
  • Psychiatry and Mental health
  • Biological Psychiatry

Cite this

Chang, Y. W., Assari, S., Prossin, A. R., Stertz, L., McInnis, M. G., & Evans, S. J. (2017). Bipolar disorder moderates associations between linoleic acid and markers of inflammation. Journal of Psychiatric Research, 85, 29-36. DOI: 10.1016/j.jpsychires.2016.10.021

Bipolar disorder moderates associations between linoleic acid and markers of inflammation. / Chang, Ya Wen; Assari, Shervin; Prossin, Alan R.; Stertz, Laura; McInnis, Melvin G.; Evans, Simon J.

In: Journal of Psychiatric Research, Vol. 85, 01.02.2017, p. 29-36.

Research output: Research - peer-reviewArticle

Chang, YW, Assari, S, Prossin, AR, Stertz, L, McInnis, MG & Evans, SJ 2017, 'Bipolar disorder moderates associations between linoleic acid and markers of inflammation' Journal of Psychiatric Research, vol 85, pp. 29-36. DOI: 10.1016/j.jpsychires.2016.10.021
Chang YW, Assari S, Prossin AR, Stertz L, McInnis MG, Evans SJ. Bipolar disorder moderates associations between linoleic acid and markers of inflammation. Journal of Psychiatric Research. 2017 Feb 1;85:29-36. Available from, DOI: 10.1016/j.jpsychires.2016.10.021
Chang, Ya Wen ; Assari, Shervin ; Prossin, Alan R. ; Stertz, Laura ; McInnis, Melvin G. ; Evans, Simon J./ Bipolar disorder moderates associations between linoleic acid and markers of inflammation. In: Journal of Psychiatric Research. 2017 ; Vol. 85. pp. 29-36
@article{a47d82f1e47247c4a1928015ce126b50,
title = "Bipolar disorder moderates associations between linoleic acid and markers of inflammation",
abstract = "Dietary polyunsaturated fatty acids (PUFA) and inflammatory proteins associate with immune activation and have been implicated in the pathophysiology of mood disorders. We have previously reported that individuals with bipolar disorder (BPD) have decreased PUFA intake, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and arachidonic acid (AA); and decreased PUFA concentration of plasma EPA and linoleic acid (LA). We have also reported an association between plasma LA and its metabolites and burden of disease measures in BPD. In the current cross-sectional study we collected blood samples and diet records from both bipolar (n = 91) and control subjects (n = 75) to quantify plasma cytokine concentrations and dietary LA intake, respectively. Using multiple linear regression techniques, we tested for case control differences in plasma cytokine levels and associations between cytokines and dietary LA intake, adjusting for sex, age, BMI, and total energy intake. We found significantly higher plasma levels of interleukin 18 (IL-18) (p = 0.036), IL-18 binding protein (IL-18BP) (p = 0.001), soluble tumor necrosis factor receptor (sTNFR) 1 (p = 0.006), and sTNFR2 (p = 0.007) in BPD compared with controls. Moreover, BPD significantly moderated the associations of dietary LA intake with plasma levels of IL-18, sTNFR1 and sTNFR2, which were inverse associations in bipolar individuals and positive associations in controls (p for dietary LA x BPD diagnosis interaction < 0.05 for all three). These findings suggest potential dysregulation of LA metabolism in BPD, which may extend to a modified influence of dietary LA on specific inflammatory pathways in individuals with BPD compared to healthy controls.",
keywords = "Bipolar disorder, Interleukin, Linoleic acid, Tumor necrosis factor receptor",
author = "Chang, {Ya Wen} and Shervin Assari and Prossin, {Alan R.} and Laura Stertz and McInnis, {Melvin G.} and Evans, {Simon J.}",
year = "2017",
month = "2",
doi = "10.1016/j.jpsychires.2016.10.021",
volume = "85",
pages = "29--36",
journal = "Journal of Psychiatric Research",
issn = "0022-3956",
publisher = "Elsevier Limited",

}

TY - JOUR

T1 - Bipolar disorder moderates associations between linoleic acid and markers of inflammation

AU - Chang,Ya Wen

AU - Assari,Shervin

AU - Prossin,Alan R.

AU - Stertz,Laura

AU - McInnis,Melvin G.

AU - Evans,Simon J.

PY - 2017/2/1

Y1 - 2017/2/1

N2 - Dietary polyunsaturated fatty acids (PUFA) and inflammatory proteins associate with immune activation and have been implicated in the pathophysiology of mood disorders. We have previously reported that individuals with bipolar disorder (BPD) have decreased PUFA intake, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and arachidonic acid (AA); and decreased PUFA concentration of plasma EPA and linoleic acid (LA). We have also reported an association between plasma LA and its metabolites and burden of disease measures in BPD. In the current cross-sectional study we collected blood samples and diet records from both bipolar (n = 91) and control subjects (n = 75) to quantify plasma cytokine concentrations and dietary LA intake, respectively. Using multiple linear regression techniques, we tested for case control differences in plasma cytokine levels and associations between cytokines and dietary LA intake, adjusting for sex, age, BMI, and total energy intake. We found significantly higher plasma levels of interleukin 18 (IL-18) (p = 0.036), IL-18 binding protein (IL-18BP) (p = 0.001), soluble tumor necrosis factor receptor (sTNFR) 1 (p = 0.006), and sTNFR2 (p = 0.007) in BPD compared with controls. Moreover, BPD significantly moderated the associations of dietary LA intake with plasma levels of IL-18, sTNFR1 and sTNFR2, which were inverse associations in bipolar individuals and positive associations in controls (p for dietary LA x BPD diagnosis interaction < 0.05 for all three). These findings suggest potential dysregulation of LA metabolism in BPD, which may extend to a modified influence of dietary LA on specific inflammatory pathways in individuals with BPD compared to healthy controls.

AB - Dietary polyunsaturated fatty acids (PUFA) and inflammatory proteins associate with immune activation and have been implicated in the pathophysiology of mood disorders. We have previously reported that individuals with bipolar disorder (BPD) have decreased PUFA intake, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and arachidonic acid (AA); and decreased PUFA concentration of plasma EPA and linoleic acid (LA). We have also reported an association between plasma LA and its metabolites and burden of disease measures in BPD. In the current cross-sectional study we collected blood samples and diet records from both bipolar (n = 91) and control subjects (n = 75) to quantify plasma cytokine concentrations and dietary LA intake, respectively. Using multiple linear regression techniques, we tested for case control differences in plasma cytokine levels and associations between cytokines and dietary LA intake, adjusting for sex, age, BMI, and total energy intake. We found significantly higher plasma levels of interleukin 18 (IL-18) (p = 0.036), IL-18 binding protein (IL-18BP) (p = 0.001), soluble tumor necrosis factor receptor (sTNFR) 1 (p = 0.006), and sTNFR2 (p = 0.007) in BPD compared with controls. Moreover, BPD significantly moderated the associations of dietary LA intake with plasma levels of IL-18, sTNFR1 and sTNFR2, which were inverse associations in bipolar individuals and positive associations in controls (p for dietary LA x BPD diagnosis interaction < 0.05 for all three). These findings suggest potential dysregulation of LA metabolism in BPD, which may extend to a modified influence of dietary LA on specific inflammatory pathways in individuals with BPD compared to healthy controls.

KW - Bipolar disorder

KW - Interleukin

KW - Linoleic acid

KW - Tumor necrosis factor receptor

UR - http://www.scopus.com/inward/record.url?scp=84993971338&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84993971338&partnerID=8YFLogxK

U2 - 10.1016/j.jpsychires.2016.10.021

DO - 10.1016/j.jpsychires.2016.10.021

M3 - Article

VL - 85

SP - 29

EP - 36

JO - Journal of Psychiatric Research

T2 - Journal of Psychiatric Research

JF - Journal of Psychiatric Research

SN - 0022-3956

ER -